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首页> 外文期刊>Journal of cardiac surgery. >Vasopressin induces rectosigmoidal mucosal ischemia during cardiopulmonary bypass
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Vasopressin induces rectosigmoidal mucosal ischemia during cardiopulmonary bypass

机译：加压素在体外循环期间诱发直肠乙状结肠黏膜缺血

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Background Lower gastrointestinal complications are rare after cardiac surgery with cardiopulmonary bypass (CPB). However, if they occur, they are associated with a high mortality. Endothelin (ET) expression and microcirculatory dysfunction have been shown to be involved in a variety of diseases of the lower gastrointestinal tract. The aim of this study was to analyze whether CPB with or without additional vasopressin administration affects the rectosigmoidal mucosal microcirculation and whether this involves the ET system. Methods Pigs were randomized in three groups (n = 6 each): I Sham, II CPB: 1 hour CPB, III CPB + vasopressin: 1 hour CPB and vasopressin (0.006 U/min kg) administration maintaining baseline arterial pressure. All animals were reperfused for 90 minutes. During the experiment hemodynamics and rectosigmoidal mucosal microcirculation were measured continuously. The rectosigmoidal mucosal expression of endothelin-1 (ET-1) and its receptor subtypes A (ETA) and B (ETB) were determined using PCR and Western blot analysis. Results CPB did not change rectosigmoidal microvascular blood flow compared to baseline (68.1 ± 4.0 vs. 75.5 ± 6.6 AU; p = 0.4), but increased ET-1 (gene, 7.8 ± 1.5 vs. 2.3 ± 0.6 RQ; p = 0.002 and protein, 12.0 ± 0.5 vs. 6.9 ± 0.3 OD mm2; p 0.001), ETA (gene, 2.3 ± 0.6 vs. 0.6 ± 0.1 RQ; p 0.001 and protein, 11.0 ± 0.3 vs. 6.2 ± 1.1 OD mm 2; p = 0.006) and ETB (gene, 6.7 ± 1.2 vs. 1.9 ± 0.3 RQ; p 0.001 and protein, 25.6 ± 1.4 vs. 14.9 ± 1.5 OD mm2; p = 0.002) expression compared to Sham. Vasopressin during CPB reduced the rectosigmoidal blood flow compared to baseline (26.5 ± 4.9 vs. 75.5 ± 6.6 AU, p 0.001), and blunted the CPB-induced increase of ET-1 (gene, 1.2 ± 0.4 RQ, p = 0.1 and protein, 8.1 ± 1.6 OD mm2, p = 0.5 vs. Sham), ETA (gene, 0.6 ± 0.1 RQ, p = 1.0 and protein, 7.0 ± 0.6 OD mm2, p = 0.6 vs. Sham) and ETB (gene, 1.3 ± 0.3 RQ, p = 0.1 and protein, 19.4 ± 2.1 OD mm2, p = 0.1 vs. Sham). Conclusion CPB does not significantly affect rectosigmoidal mucosal microcirculation; however, it upregulates ET-1, ETA, and ETB. Vasopressin blunts the CPB-induced elevation of ET-1, ETA, and ETB and induces rectosigmoidal mucosal ischemia during CPB.
机译：背景技术在进行体外循环（CPB）的心脏手术后，较低的胃肠道并发症很少见。然而，如果它们发生，则它们与高死亡率有关。内皮素（ET）的表达和微循环功能障碍已被证明与下消化道的多种疾病有关。这项研究的目的是分析加或不加其他加压素的CPB是否会影响直肠乙状结肠粘膜微循环以及这是否涉及ET系统。方法将猪随机分为三组（每组6只）：I Sham，II CPB：1小时CPB，III CPB +血管加压素：1小时CPB和抗血管加压素（0.006 U / min kg），维持基线动脉压。将所有动物再灌注90分钟。在实验过程中，连续测量血流动力学和直肠乙状结肠粘膜微循环。使用PCR和蛋白质印迹分析确定内皮素-1（ET-1）及其受体亚型A（ETA）和B（ETB）在直肠乙状结肠粘膜中的表达。结果CPB与基线相比没有改变直肠乙状结肠微血管的血流量（68.1±4.0 vs. 75.5±6.6 AU; p = 0.4），但ET-1增加（基因，7.8±1.5 vs. 2.3±0.6 RQ; p = 0.002和蛋白质，12.0±0.5 vs. 6.9±0.3 OD mm2; p <0.001），ETA（基因，2.3±0.6 vs. 0.6±0.1 RQ; p <0.001和蛋白质，11.0±0.3 vs. 6.2±1.1 OD mm 2; p = 0.006）和ETB（基因，6.7±1.2 vs. 1.9±0.3 RQ; p <0.001和蛋白质，25.6±1.4 vs. 14.9±1.5 OD mm2; p = 0.002）表达与Sham相比。与基线相比，CPB期间的加压素减少了直肠乙状结肠血流量（26.5±4.9 vs. 75.5±6.6 AU，p <0.001），并减弱了CPB诱导的ET-1的增加（基因，1.2±0.4 RQ，p = 0.1和蛋白质，8.1±1.6 OD mm2，p = 0.5 vs.Sham），ETA（基因，0.6±0.1 RQ，p = 1.0和蛋白质，7.0±0.6 OD mm2，p = 0.6 vs.Sham）和ETB（基因，1.3 ±0.3 RQ，p = 0.1和蛋白质，19.4±2.1 OD mm2，p = 0.1 vs.Sham）。结论CPB对直肠乙状结肠黏膜微循环无明显影响。但是，它会上调ET-1，ETA和ETB。加压素能使CPB引起的ET-1，ETA和ETB升高而钝化，并在CPB期间引起直肠乙状结肠粘膜缺血。

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